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Updated: Oct 8, 2025

Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
Published on: June 23, 2022
SOCS2 expression in hematopoietic and non-hematopoietic cells during Trypanosoma cruzi infection: Correlation with
Paulo Gaio1, Melisa Gualdrón-López2, Allysson Cramer1
1Department of Biochemistry and Immunology, Institute of Biological Science, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Abstract:
Chagas disease has a complex pathogenesis wherein the host immune response is essential for controlling its development. Suppressor of cytokine signaling(SOCS)2 is a crucial protein that regulates cytokine production. In this study, SOCS2 deficiency resulted in an initial imbalance of IL12- and IL-10-producing neutrophils and dendritic cells (DCs), which caused a long-lasting impact reducing inflammatory neutrophils and DCs, and tolerogenic DCs at the peak of acute disease. A reduced number of inflammatory and pro-resolving macrophages, and IL17A-producing CD4+ T cells, and increased lymphocyte apoptosis was found in SOCS2-deficient mice. Electrocardiogram analysis of chimeric mice showed that WT mice that received SOCS2 KO bone marrow transplantation presented increased heart dysfunction. Taken together, the results demonstrated that SOCS2 is a crucial regulator of the immune response during Trypanosoma cruzi infection, and suggest that a SOCS2 genetic polymorphism, or failure of its expression, may increase the susceptibility of cardiomyopathy development in Chagasic patients.
Insights
Suppressor of cytokine signaling 2 (SOCS2) deficiency impairs immune responses to Chagas disease. SOCS2 loss in mice led to cardiac dysfunction, suggesting a link between SOCS2 and Chagasic cardiomyopathy susceptibility.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Chagas disease pathogenesis involves complex host immune responses.
- Suppressor of cytokine signaling 2 (SOCS2) is vital for regulating cytokine production.
Purpose of the Study:
- To investigate the role of SOCS2 in the immune response to Trypanosoma cruzi infection.
- To determine the impact of SOCS2 deficiency on Chagas disease development and cardiomyopathy.
Main Methods:
- Studied SOCS2-deficient mice and chimeric mice with SOCS2 knockout bone marrow transplantation.
- Analyzed immune cell populations (neutrophils, dendritic cells, macrophages, T cells) and lymphocyte apoptosis.
- Performed electrocardiogram analysis to assess cardiac function.
Main Results:
- SOCS2 deficiency caused initial immune cell imbalance, affecting neutrophils and dendritic cells.
- Reduced inflammatory and regulatory immune cells, increased lymphocyte apoptosis in SOCS2-deficient mice.
- SOCS2 knockout bone marrow transplantation into wild-type mice exacerbated heart dysfunction.
Conclusions:
- SOCS2 is a critical regulator of the immune response during Trypanosoma cruzi infection.
- SOCS2 genetic variations may increase susceptibility to Chagasic cardiomyopathy.
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